OBJECTIVE: The expression pattern of lymphocyte function-associated antigen 3 (LFA-3) in the buccal mucosa of oral lichen planus (OLP) patients was compared to that of healthy controls to investigate the possible role of LFA-3 in cell interactions within OLP lesions. MATERIALS AND METHODS: Samples of buccal mucosa from 17 clinically healthy individuals and 17 OLP lesions were analysed. Expression of LFA-3, CD2, CD3 and CD14 was visualized by an immunoperoxidase technique and assessed microscopically. RESULTS: In healthy buccal mucosa LFA-3 was expressed on keratinocytes, Langerhans cells within the epithelium and on endothelial cells in the lamina propria. In OLP patients a similar pattern of LFA-3 staining was observed. In addition, cytoplasmic LFA-3 without accompanying surface staining, was seen on a subpopulation of macrophage-like cells. Substantial amounts of LFA-3 also appeared to be associated with non-cellular components of the extracellular matrix within the inflammatory infiltrate. CONCLUSIONS: We have obtained evidence for a previously undescribed localization of LFA-3 within macrophages, and have observed that expression of LFA-3 is apparently elevated within OLP lesions. LFA-3 may play an important role in the pathogenesis of OLP.
OBJECTIVE: The expression pattern of lymphocyte function-associated antigen 3 (LFA-3) in the buccal mucosa of oral lichen planus (OLP) patients was compared to that of healthy controls to investigate the possible role of LFA-3 in cell interactions within OLP lesions. MATERIALS AND METHODS: Samples of buccal mucosa from 17 clinically healthy individuals and 17 OLP lesions were analysed. Expression of LFA-3, CD2, CD3 and CD14 was visualized by an immunoperoxidase technique and assessed microscopically. RESULTS: In healthy buccal mucosa LFA-3 was expressed on keratinocytes, Langerhans cells within the epithelium and on endothelial cells in the lamina propria. In OLP patients a similar pattern of LFA-3 staining was observed. In addition, cytoplasmic LFA-3 without accompanying surface staining, was seen on a subpopulation of macrophage-like cells. Substantial amounts of LFA-3 also appeared to be associated with non-cellular components of the extracellular matrix within the inflammatory infiltrate. CONCLUSIONS: We have obtained evidence for a previously undescribed localization of LFA-3 within macrophages, and have observed that expression of LFA-3 is apparently elevated within OLP lesions. LFA-3 may play an important role in the pathogenesis of OLP.